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PUBLIC HEALTH GOALS FOR CHEMICALS IN DRINKING WATER
RADIUM-226 and -228 March 2006 Governor of the State of
California Arnold Schwarzenegger Secretary for Environmental
Protection California Environmental Protection Agency Alan C.
Lloyd, Ph.D. Director Office of Environmental Health Hazard
Assessment Joan E. Denton, Ph.D.
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Public Health Goal for
Radium-226 and -228 in Drinking Water
Prepared by
Office of Environmental Health Hazard Assessment California
Environmental Protection Agency
Pesticide and Environmental Toxicology Branch
Anna M. Fan, Ph.D., Chief
Deputy Director for Scientific Affairs George V. Alexeeff,
Ph.D.
March 2006
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LIST OF CONTRIBUTORS
PHG PROJECT MANAGEMENT
Project Director Anna Fan, Ph.D.
PHG Program Leader Robert Howd, Ph.D.
Comment Coordinator Catherine Caraway, B.S.
Revisions/Responses Robert Howd, Ph.D.
REPORT PREPARATION
Author Javier Avalos, Ph.D.
Primary Reviewers Brian Endlich, Ph.D. Charles Vidair, Ph.D.
Final ReviewersAnna Fan, Ph.D.
George Alexeeff, Ph.D. Robert Howd, Ph.D.
SUPPORT
Administrative Support
Genevieve Vivar Sharon Davis
Hermelinda Jimenez
Library Support Charleen Kubota, M.L.S.
Web site Posting
Laurie Monserrat
The contributions of S. Cohen and Associates, McLean, VA, to
development of this document, under contract with the State of
California, are gratefully acknowledged.
We thank the U.S. Environmental Protection Agency (Office of
Water; National Center for Environmental Assessment) and the
faculty members of the University of
California with whom the Office of Environmental Health Hazard
Assessment contracted through the University of California Office
of the President for their peer
reviews of the public health goal documents, and gratefully
acknowledge the comments received from all interested parties.
Radium-226 and 228 in Drinking Water California Public Health
Goal iii March 2006
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PREFACE
Drinking Water Public Health Goal Pesticide and Environmental
Toxicology Branch
Office of Environmental Health Hazard Assessment California
Environmental Protection Agency
This Public Health Goal (PHG) technical support document
provides information on health effects from contaminants in
drinking water. PHGs are developed for chemical contaminants based
on the best available toxicological data in the scientific
literature. These documents and the analyses contained in them
provide estimates of the levels of contaminants in drinking water
that would pose no significant health risk to individuals consuming
the water on a daily basis over a lifetime.
The California Safe Drinking Water Act of 1996 (Health and
Safety Code, Section 116365) requires the Office of Environmental
Health Hazard Assessment (OEHHA) to perform risk assessments and
adopt PHGs for contaminants in drinking water based exclusively on
public health considerations. The Act requires that PHGs be set in
accordance with the following criteria:
1. PHGs for acutely toxic substances shall be set at levels at
which no known or anticipated adverse effects on health will occur,
with an adequate margin of safety.
2. PHGs for carcinogens or other substances that may cause
chronic disease shall be based solely on health effects and shall
be set at levels that OEHHA has determined do not pose any
significant risk to health.
3. To the extent the information is available, OEHHA shall
consider possible synergistic effects resulting from exposure to
two or more contaminants.
4. OEHHA shall consider potential adverse effects on members of
subgroups that comprise a meaningful proportion of the population,
including but not limited to infants, children, pregnant women, the
elderly, and individuals with a history of serious illness.
5. OEHHA shall consider the contaminant exposure and body burden
levels that alter physiological function or structure in a manner
that may significantly increase the risk of illness.
6. OEHHA shall consider additive effects of exposure to
contaminants in media other than drinking water, including food and
air, and the resulting body burden.
7. In risk assessments that involve infants and children, OEHHA
shall specifically assess exposure patterns, special
susceptibility, multiple contaminants with toxic mechanisms in
common, and the interactions of such contaminants.
Radium-226 and 228 in Drinking Water California Public Health
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8. In cases of insufficient data for OEHHA to determine a level
that creates no significant risk, OEHHA shall set the PHG at a
level that is protective of public health with an adequate margin
of safety.
9. In cases where scientific evidence demonstrates that a safe
dose response threshold for a contaminant exists, then the PHG
should be set at that threshold.
10. The PHG may be set at zero if necessary to satisfy the
requirements listed above in items seven and eight.
11. PHGs adopted by OEHHA shall be reviewed at least once every
five years and revised as necessary based on the availability of
new scientific data.
PHGs adopted by OEHHA are for use by the California Department
of Health Services (DHS) in establishing primary drinking water
standards (State Maximum Contaminant Levels, or MCLs). Whereas PHGs
are to be based solely on scientific and public health
considerations without regard to economic cost considerations or
technical feasibility, drinking water standards adopted by DHS are
to consider economic factors and technical feasibility. Each
primary drinking water standard adopted by DHS shall be set at a
level that is as close as feasible to the corresponding PHG,
placing emphasis on the protection of public health. PHGs
established by OEHHA are not regulatory in nature and represent
only non-mandatory goals. By state and federal law, MCLs
established by DHS must be at least as stringent as the federal
MCL, if one exists.
PHG documents are used to provide technical assistance to DHS,
and they are also informative reference materials for federal,
state and local public health officials and the public. While the
PHGs are calculated for single chemicals only, they may, if the
information is available, address hazards associated with the
interactions of contaminants in mixtures. Further, PHGs are derived
for drinking water only and are not intended to be utilized as
target levels for the contamination of other environmental
media.
Additional information on PHGs can be obtained at the OEHHA Web
site at www.oehha.ca.gov.
Radium-226 and 228 in Drinking Water California Public Health
Goal v March 2006
www.oehha.ca.gov.
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TABLE OF CONTENTS
LIST OF CONTRIBUTORS
..................................................................................III
PREFACE
................................................................................................................
IV
TABLE OF CONTENTS
...........................................................................................
I
PUBLIC HEALTH GOAL FOR RADIUM-226 AND RADIUM-228 IN DRINKING
WATER
.................................................................................................1
SUMMARY.................................................................................................................1
INTRODUCTION
......................................................................................................1
CHEMICAL PROFILE
.............................................................................................3
Chemical
Identity..............................................................................................3
Physical and Chemical Properties
....................................................................5
Source
...............................................................................................................5
ENVIRONMENTAL OCCURRENCE AND HUMAN EXPOSURE
...................5
Air
.....................................................................................................................5
Soil
....................................................................................................................5
Water.................................................................................................................6
Food
..................................................................................................................8
METABOLISM AND PHARMACOKINETICS
....................................................9
Absorption
........................................................................................................9
Metabolism
.....................................................................................................10
Distribution
.....................................................................................................10
Excretion.........................................................................................................11
Mechanism of Action
.....................................................................................13
TOXICOLOGY
........................................................................................................13
Toxicological Effects in Animals and
Plants..................................................13
Acute Toxicity
..........................................................................................13
Subchronic
Toxicity..................................................................................14
Genetic Toxicity
.......................................................................................14
Radium-226 and 228 in Drinking Water California Public Health
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Developmental and Reproductive Toxicity
..............................................14
Immunotoxicity.........................................................................................15
Neurotoxicity
............................................................................................15
Chronic Toxicity and
Carcinogenicity......................................................15
Toxicological Effects in Humans
...................................................................15
Acute Toxicity
..........................................................................................15
Subchronic
Toxicity..................................................................................16
Genetic Toxicity
.......................................................................................16
Developmental and Reproductive Toxicity
..............................................17
Immunotoxicity.........................................................................................17
Neurotoxicity
............................................................................................17
Chronic
Toxicity.......................................................................................17
Carcinogenicity.........................................................................................17
DOSE-RESPONSE
ASSESSMENT........................................................................19
Noncarcinogenic
Effects.................................................................................19
Carcinogenic
Effects.......................................................................................20
CALCULATION OF PHG
......................................................................................22
Noncarcinogenic
Effects.................................................................................22
Carcinogenic
Effects.......................................................................................24
RISK CHARACTERIZATION
..............................................................................25
OTHER REGULATORY
STANDARDS...............................................................25
REFERENCES
.........................................................................................................28
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PUBLIC HEALTH GOAL FOR RADIUM-226 AND RADIUM-228 IN DRINKING
WATER
SUMMARY The Office of Environmental Health Hazard Assessment
(OEHHA) hereby establishes Public Health Goals (PHGs) of 0.05 pCi/L
and 0.019 pCi/L for radium-226 and radium-228, respectively, in
drinking water. These PHG values are based on the known
carcinogenic effects of radiation observed in humans. The risk
estimates for these isotopes utilize the U.S. Environmental
Protection Agency (U.S. EPA) report, Cancer Risk Coefficients for
Environmental Exposure to Radionuclides: Federal Guidance Report
13, published in 1999. This U.S. EPA report on the relative risks
of radioactive substances to humans was produced specifically to
provide technical guidance to federal and state risk assessors. The
report provides tabulated risk coefficients based on
state-of-the-art methods and models that take into account many
factors, including age, gender, competing causes of death, and the
risks from water ingestion alone. The estimation of the risk
coefficients (carcinogenic potencies) assumes the linear
no-threshold model and is especially appropriate for estimating
cancer risks at low levels of exposure to radionuclides like radium
and strontium. OEHHA used the information provided by U.S. EPA in
Federal Guidance Report 13 to calculate the PHGs for radium-226 and
radium-228 by applying the risk coefficients, based on carcinogenic
effects observed in radium dial painters, for these radium isotopes
to a lifetime of exposure to 2 L/day of drinking water. The PHG
values assume a de minimis excess individual cancer risk level of
10-6 from exposure to radium.
Public health-protective concentrations for noncancer effects
were calculated based on bone necrosis in a human population with
less-than-lifetime exposures to radium. In this case, the primary
human population used for these assessments was the former radium
dial painters, whose median age was 18. Using values based on
children’s exposures, with a combined uncertainty factor of ten,
the health-protective concentrations were estimated as 200 pCi/L
for both radium-226 and radium-228. The concentrations estimated to
protect against cancer (above) would also be adequate to protect
against all non-cancer effects.
The U.S. EPA Maximum Contaminant Level (MCL) for radium in
community water supplies, combined for radium-226 and -228, is 5
pCi/L (U.S. EPA, 1976). The California MCL, established in 1997, is
also 5 pCi/L for the combined isotopes (DHS, 2005a).
INTRODUCTION This PHG technical support document provides
information on health effects from radium-226 and radium-228
(226Ra, 228Ra) in drinking water. PHGs are developed for
contaminants based on the best available toxicological data in the
scientific literature. These documents and the analysis contained
in them provide estimates of the levels of
Radium-226 and 228 in Drinking Water California Public Health
Goal 1 March 2006
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contaminants in drinking water that would pose no significant
health risk to individuals consuming the water on a daily basis
over a lifetime.
This PHG technical support document addresses two radioactive
isotopic forms of radium. Radioactivity is produced by unstable
nuclei, and isotopes of elements with this property are called
radionuclides. The instability in the nucleus is manifested as the
potential to decay or fall into a lower energy state by releasing
principally either alpha or beta particles, or gamma rays. An alpha
particle is defined as a positively charged particle consisting of
two protons and two neutrons. A beta particle is either a
negatively charged negatron/electron or a positively charged
particle (positron). Gamma rays are high energy, short-wavelength
electromagnetic radiation. Radioactive emissions are measured by an
activity unit called a curie (Ci), representing 3.7 x 1010 nuclear
disintegrations per second. For drinking water, the common
representation of activity is the picocurie (pCi), equal to 10-12
Ci. Another presentation of radioactivity in the International
System of Units is the becquerel (Bq), which is defined as one
disintegration per second. Energetic atoms of radionuclides release
their energy either through ejection of particles or emission of
electromagnetic radiation, which then interact with other atoms or
matter, particularly to knock electrons out of their orbits around
the nucleus. This process is defined as ionizing radiation.
Ionizing radiation is a particular concern for living tissues as it
could lead to alterations in the important constituents of the cell
including DNA, resulting in changes in structure and function of
the cells or organ systems. Understanding the potential for
ionizing radiation to effect changes to cells and tissues requires
knowing how much energy is deposited in the tissues as a result of
these emissions. This concept is referred to as the absorbed dose
and is represented by units of rad (radiation absorbed dose), which
is the amount of energy (in units of 100 ergs) deposited in one
gram of matter or tissue. In International Units, the gray (Gy) is
used for characterizing absorbed dose, representing one joule/kg of
energy deposited. One gray is equivalent to 100 rad. However, the
radiation particles or energy types differ in their ability to
affect tissues, and thus an adjustment or quality factor can be
used to compensate for the differences. For example, an alpha
particle deposits its energy in a short range and rarely can
penetrate the surface layers of tissues, while beta particle and
gamma radiation deposit their energies over a greater range. The
rem (roentgen equivalent man) unit accounts for the difference in
the type of radiation by multiplying the absorbed dose in rads by a
quality factor. Rem can also be represented by the unit, sieverts
(Sv), equaling 100 rems. Another fine-tuning of the absorbed dose
is to adjust for the different types of organs affected by
radioactive emissions; this is referred to as rem-ede (effective
dose-equivalent).
The radionuclides 226Ra and 228Ra are naturally occurring. They
are formed from the decay of the primordial radionuclides
uranium-238 and thorium-232, respectively, in the earth’s crust. As
such, there is a small amount of 226Ra and 228Ra in most
environmental media including drinking water. 226Ra decays by
emitting an alpha particle, and 228Ra decays by beta particle
emissions, in both cases accompanied by gamma emissions.
Radium-226 and 228 in Drinking Water California Public Health
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The federal government has regulated the levels of 226Ra and
228Ra in community water supplies since the mid-1970s. The U.S. EPA
promulgated Maximum Contaminant Levels (MCLs) for radium and other
radionuclides in community water supplies in their 1976 National
Interim Primary Drinking Water Regulation (U.S. EPA, 1976). The
combined MCL for 226Ra and 228Ra is 5 pCi/L.
In 1991, the U.S. EPA proposed new MCLs for 226Ra and 228Ra at
20 pCi/L each based on newer dosimetry (U.S. EPA, 1991). The
proposed rule was never implemented.
In 2000, the U.S. EPA finalized their rule for drinking water
(U.S. EPA, 2000, 2002). For 226Ra and 228Ra the MCL remains at 5
pCi/L (combined) because updated dosimetry and risk levels yielded
similar concentrations (U.S. EPA, 2005a). The U.S. EPA estimates
the lifetime cancer risk at this level of radioactivity derived
from radium to be 1 x 10-4 (U.S. EPA, 1991). However, U.S. EPA
withdrew the carcinogenicity assessment for lifetime exposure
calculation in the Integrated Risk Information System (IRIS) in
1991 (U.S. EPA, 2005b), pending further review by the CRAVE Agency
Work Group. The IRIS Web site reports that a screening-level review
conducted by an EPA contractor of the more recent toxicology
literature pertinent to the cancer assessment for radium 226 and
radium 228 conducted in September 2002 did not identify any
critical new studies.
Other agencies have developed health protective levels for
radium. The purpose of this document is to review the evidence on
toxicity of 226Ra and 228Ra and to derive a PHG for them in
drinking water based on a de minimis risk level.
CHEMICAL PROFILE
Chemical Identity
Radium-226 is a naturally-occurring radioactive isotope that is
formed from the decay of uranium-238, a primordial radionuclide.
226Ra decays with a half-life of 1622 years to radon-222 and emits
an alpha particle (an energetic helium nucleus) in the decay
process. The energy of the alpha particles is 4.6 million electron
volts (MeV) for approximately 6 percent of the decays and 4.78 MeV
for approximately 94 percent of the decays, which is sufficient to
produce ionizations and excitations of molecules in the path of the
alpha particles. The average range of these alpha particles in air
is about 0.5 cm and about a thousand-fold less in water and tissue
(approximately 6 μm). Because alpha particles impart a large amount
of energy in a very short distance compared to other types of
ionizing radiation (beta and photon), radium-226 poses a relatively
large hazard to humans when taken internally. Table 1 summarizes
some of the more important characteristics of 226Ra.
Radium-226 and 228 in Drinking Water California Public Health
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Table 1. Characteristics of Radium-226
Properties Value Atomic number 88 Atomic mass 226 Half-life 1622
years Decay constant 4.3 x 10-4 per year Characteristics of alpha
particle Energy 4.78 MeV (94%), 4.6 MeV (6%) Average track length
0.5 cm (air) Specific activity 0.988 Ci/g
Radium-228 is a naturally-occurring radioactive isotope that is
formed from the decay of thorium-232, a primordial radionuclide.
228Ra decays with a half-life of 5.7 years to actinium-228 and
emits a beta particle (an energetic electron) in the decay process.
The energy of the beta particles (maximum 55 kiloelectron volts
(keV), average 14 keV) is sufficient to produce ionizations and
excitations of molecules in their path. The average range of these
beta particles in air is less than 1 μm in water. Because beta
particles travel such short distances in water and tissue, 228Ra
poses a radiation hazard to humans only when taken internally.
Table 2 summarizes some of the more important characteristics of
228Ra.
Table 2. Characteristics of Radium-228
Properties Value
Atomic number 88 Atomic mass 228 Half-life 5.7 years Decay
constant 0.12 per year Characteristics of beta particle Average
energy 14 keV Average track length
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Physical and Chemical Properties
The chemical properties of radium are similar to other alkaline
earth elements, particularly barium and calcium. Radium exists in
only the +2 oxidation state in solution and does not easily complex
in water (Ames and Rai, 1978). The carbonate and sulfate salts of
radium are very insoluble in water. The chloride, nitrate and
bromide forms are soluble.
Water concentrations of radium appear to be controlled by
dissolution and sorption (U.S. EPA, 1991). Sorption can remove
radium from solution by adsorption and coprecipitation by
scavengers such as iron hydroxide and barium sulfate. Radium is
most mobile in aquifers with high concentrations of dissolved
solids (Benes et al., 1984, 1985).
Source
Radium is a naturally–occurring silvery white radioactive metal
(atomic number 88) that is formed from the radioactive decay of
uranium and thorium. It can exist in several isotopes, radium-226
(226Ra), radium-228 (228Ra), radium-224 (224Ra), and radium-223
(223Ra). 226Ra and 228Ra are the isotopes of primary environmental
concern, because their half-lives are long enough to promote
substantial environmental accumulation. The half-life of 226Ra is
about 1,600 years, and the half-life for 228Ra is about 6 years.
226Ra is part of the uranium-238 decay series and decays to
radon-222 by alpha particle emission. 228Ra is a progeny of
thorium-232 and decays to actinium-228 by emitting a beta
particle.
ENVIRONMENTAL OCCURRENCE AND HUMAN EXPOSURE
Radium is nearly ubiquitous at low concentrations in air, water,
soil, rock, and food. The median concentrations of 226Ra and 228Ra
in drinking water are generally low, but there are regions where
higher concentrations are known to occur. The mining of coal and
uranium ore and their use in energy production has resulted in the
redistribution of radium in the environment, but the overall effect
appears small.
Air
Radium, being a non-gaseous element, is present in the air at
extremely low levels, as a constituent of aerosols and suspended
matter. The U.S. EPA reported outdoor concentrations of about 1.5 x
10-5 pCi 226Ra /m3 and 2.3 x 10-3 pCi 228Ra /m3 (U.S. EPA, 1991).
Dust samples collected from the atmosphere of New York City were
found to contain 226Ra at 8 x 10-5 pCi/m3 (3.0 x 10-6 Bq/m3) and
228Ra at 1.5 x 10-4 pCi/m3 (5.6 x 10-6 Bq/m3) (ATSDR, 1990).
Soil
Radium-226 and Radium-228 can be found in soil throughout the
country. Myrick et al. (1981) reported the mean concentration of
226Ra in 356 surface soil samples collected Radium-226 and 228 in
Drinking Water California Public Health Goal 5 March 2006
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from 33 states was 1.1 pCi/g (0.041 Bq/g). This mean
concentration is very similar to those for 226Ra reported by
Eisenbud (1973) for typical igneous rock, 1.3 pCi/g (0.048 Bq/g).
Concentrations by rock type included the following:
• Sandstone, 0.71 pCi/g (0.026 Bq/g)
• Limestone, 0.42 pCi/g (0.016 Bq/g)
• Shale, 1.1 pCi/g (0.41 Bq/g)
Coal burning and uranium mining/milling operations have produced
elevated levels of radium in soil. Kalin (1988), Landa (1984), and
Tracy et al. (1983) reported the concentration of 226Ra in soils
that were contaminated by mining and milling activities to range
from 1 to 37,000 pCi/g (0.037 to 137 Bq/g).
Using uranium concentrations as an indicator of radium levels,
national radioactivity surveys indicate that elevated radium levels
in soil are expected in the Western third of the continental U.S.,
including large areas of California and Idaho (ATSDR, 1990). In
addition, these surveys predict elevated levels of radium in
Wisconsin, Minnesota, the Appalachian Mountains, and Florida.
Water
Various studies investigated the occurrence of radium in ground,
surface, and treated drinking water (Aieta et al., 1987; Cech et
al., 1988; U.S. EPA, 1985; Hess et al., 1985; Longtin, 1988; Lucas,
1985; Michel and Cothern, 1986; USGS, 1998; Watson et al., 1884).
In general, shallow groundwater has less radium than deep aquifers,
and treated water has less radium than raw groundwater. The radium
content of surface water is usually very low, lower than most
groundwater supplies.
Radium-226, a progeny of U-238, is more commonly found in
groundwater than 228Ra a progeny of thorium-232 because uranium has
a relatively higher solubility than thorium. The geochemical
properties of 226Ra differ from those of U-238, and co-occurrence
is not common (USGS, 1998) because the degree and chemical
conditions of mobilization of the parent and progeny are
different.
The most extensive region in the nation where 226Ra occurs in
elevated concentrations in groundwater is in north central states
including Minnesota, Wisconsin, Illinois, Iowa, and Missouri (USGS,
1998). In these states, drinking water is drawn from deep aquifers
that tend to have limited sorption sites, and radium solubility is
enhanced by the ionic effect of high dissolved solids.
Radium-226 is also found at high levels in water derived from
aquifers in the east from New Jersey to Georgia (USGS, 1998). These
aquifers are composed of unconsolidated sand that contain
uranium-bearing minerals. This sand also tends to have limited
sorption capacity, enhancing the solubility of radium.
Although 228Ra is chemically similar to 226Ra, its distribution
in groundwater is very different for several reasons. The
relatively short half-life of 228Ra limits the potential for
transport without the parent being present. Consequently, 228Ra
cannot migrate far from its source before it decays to another
progeny. Thorium-232, the parent of 228Ra, is
Radium-226 and 228 in Drinking Water California Public Health
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extremely insoluble and is not subject to mobilization in most
groundwater environments (USGS, 1998). The insolubility of thorium
(unlike uranium) limits the distribution of 228Ra in groundwater.
Areas associated with the presence of 228Ra include the East
coastal plain and high plains aquifers.
Several nation-wide surveys measured the levels of 226Ra and
228Ra in the nation’s drinking water supply (U.S. EPA, 1986, 1988,
1997; Longtin, 1988; and USGS, 1998). The U.S. EPA considers the
National Inorganics and Radionuclide Survey (NIRS, U.S. EPA, 1988),
performed by the Office of Drinking Water, to be the most suitable
for deriving estimates of national radium concentrations in
drinking water (U.S. EPA, 1990). Table 3 below summarizes the
findings of the NIRS.
Table 3. Summary of Radium Concentrations (pCi/L) Measured in
Drinking Water in the National Inorganics and Radionuclide Survey
(NIRS) (U.S. EPA, 1988)
Radionuclide Mean Maximum Number ofSamples
226Ra 0.4 15 990 228Ra 0.7 12 990
Most recently, the U.S. Geological Survey (USGS) performed a
reconnaissance survey to provide additional information concerning
radium in drinking water. This survey was designed to assess the
co-occurrence of the different radium isotopes in the nation’s
drinking water supply (USGS, 1998). They found poor correlation
between the concentrations of 226Ra and 228Ra, but co-occurrence is
common, as described below for 525 out of 707 water sources in
California. Table 4 below summarizes the radium concentrations
measured by the USGS reconnaissance survey.
Table 4. Summary of Radium Concentrations (pCi/L) in Drinking
Water from the USGS Reconnaissance Survey (USGS, 1998)
Radionuclide Mean Median Standard Deviation Maximum Number
of
samples 226Ra 1.6 0.4 2.8 16.9 99 228Ra 2.1 0.5 7.9 72.3 99
The State of California has measured over 19,600 public drinking
water sources from 1984 to 2000 for various radioactive
contaminants. 226Ra and 228Ra were detected in only about ten
percent of the water sources, presumably those that were judged to
have the most potential for significant contamination. Radium-226
was found in 427 of the 1,369 sampled sources, 228Ra in 146 of the
571 sampled sources, and 226Ra + 228Ra (specific radioactivity not
distinguished) in 525 out of 707 sampled sources (DHS, 2005a). The
MCL of 5 pCi/L was exceeded 100 times in this time period (1984 to
2000) (DHS,
Radium-226 and 228 in Drinking Water California Public Health
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2005b). For 2001, there were four wells with a level of
radium-228 that exceeded the MCL while only one well was found with
a radium-226 level greater than the MCL (DHS, 2005c).
Food
Radium occurs in many different foods, and the reported
concentrations vary considerably. Eisenbud (1973) estimated the
mean 226Ra content of diets in 11 U.S. cities to be between 0.52 to
0.73 pCi/kg (0.019 to 0.027 Bq/kg). Watson et al. (1984) estimated
the mean concentrations of 226Ra in milk and beef to be about 0.23
pCi/L and 0.22 pCi/kg, respectively.
The U.S. EPA reported that eggs, pasta, bread and other bakery
products, and potatoes are the major source of 226Ra in the diet
(U.S. EPA, 1991). They estimated the average adult dietary intake
of 226Ra and 228Ra to be between 1 and 2 pCi/day, and that drinking
water supplies would contribute less than 50 percent of the total
intake. The value of 0.5 will be used as the relative source
contribution (RSC) in the calculation of the non-carcinogenic
public-health protective concentration.
The National Council on Radiation Protection and Measurements
(NCRP) found a similar pattern in intake levels of 226Ra and 228Ra
for three U.S. cities, where dietary intake was greater from food
sources than from water (NCRP, 1975). Their results are summarized
in Table 5. The low levels of radium in drinking water in these
three cases may be related to derivation of drinking water from
surface sources rather than groundwater.
Table 5. Estimates of Total Dietary Intake (pCi/d) of 226Ra and
228Ra (NCRP, 1975) 226Ra 228Ra
New York San Francisco San Juan New York San
Francisco Cereals and grain products
0.56 0.39 0.14 0.42 0.37
Meat, fish, eggs 0.46 0.07 0.01 0.14 0.08 Milk and dairy
products
0.14 0.05 0.02 0.05 0.10
Green vegetables and fruits
0.54 0.24 0.53 0.44 0.38
Root vegetables 0.06 0.04 - 0.12 0.08 Water 0.02 0.03 0.01 Total
1.78 0.85 0.71 1.2 1.0
Radium-226 and 228 in Drinking Water California Public Health
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METABOLISM AND PHARMACOKINETICS In the United States, the
radiation protection community uses the recommendations of the
International Commission on Radiological Protection (ICRP) for its
dosimetric, metabolic and biokinetic models for radionuclides. Most
recently, the federal government adopted the new age-specific
biokinetic models of the ICRP (U.S. EPA, 2000), and these models
are described in a series of documents published between 1989 and
1996 (ICRP, 1989, 1993, 1995ab, 1996). We used the metabolic and
pharmacokinetic information in these ICRP documents to summarize
what is known about the absorption, distribution, and excretion of
radium.
Absorption
The ICRP estimated that gastrointestinal absorption of radium is
about 15-21 percent of the ingested amount based on data for whole
body 226Ra in adult humans who drank water high in 226Ra for
extended periods or ingested 226Ra incorporated in food (ICRP,
1993). Normal elderly human subjects that ingested mock radium dial
paint containing 224Ra absorbed approximately 20 percent of
ingested radium as an average (Maletskos et al., 1966, 1969). In a
study in which an adult human male took 0.05 mg radium by mouth on
two occasions, an estimated 25 to 35 percent of the ingested amount
remained in the body at 5-6 days (Siel, 1915). In rats, fasting for
18 hours increased absorption of radium in young adult males
(Taylor, 1962). For radium, the ICRP adopted a gut to blood
transfer factor value (f1) of 0.2 for adults (ICRP, 1993).
There is considerable evidence of elevated gastrointestinal
absorption of the alkaline earth elements by both laboratory
animals and humans during periods of rapid growth, but there is
relatively little radium-specific information (ICRP, 1993).
Scientists report results that suggest that dietary 226Ra is
transferred to the bone at a higher rate during periods of rapid
growth than during adulthood or periods of slow growth (Muth and
Globel, 1983). Taylor et al. (1962) estimated that radium
absorption in suckling rats was 79 percent, and absorption in young
adult and old rats was 11 percent and 3 percent, respectively. Data
from a beagle study suggest considerably greater radium absorption
in immature individuals (Della Rosa et al., 1967). Because of this
information and information from other alkaline earth elements,
particularly strontium, the ICRP recommend f1 values of 0.6 for
infants and 0.3 for ages 1-15 (ICRP, 1993).
Biokinetic models mathematically characterize the movement,
translocation, fate, deposition, and excretion of a substance in a
living system. Such models predict where substances go in the body,
and how long they remain, which permits the calculation of internal
dose and risk to specific tissues and organs as well as the whole
body. In the dose computation scheme of the ICRP, information on
the biological behavior of radionuclides is contained in three
types of biokinetic models: a respiratory model, a gastrointestinal
model (GI), and an element-specific systemic model.
The GI model is used to describe the movement of swallowed or
endogenously secreted material through the stomach and intestines.
Element specific gut-to-blood transfer factors (f1) quantify the
amount absorbed from the small intestine to the blood (U.S. EPA,
2000). The GI model developed by the ICRP divides the GI tract into
four
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compartments: stomach, small intestine, upper large intestine,
and lower large intestine. The ICRP assumes first-order transfer of
material from one compartment to the next using simple mass balance
and rate equations. The model assumes that absorption to the blood
occurs only in the small intestine.
Absorption of radium after inhalation exposure has also been
reported. Marinelli et al. (1953) found radium deposited both in
the lungs and the skeleton of individuals who were exposed to
radium following the accidental rupture of capsules containing
radium sulfate (presumed to be primarily 226radium). However, it is
not clear if the radium that entered the systemic circulation was
due to inhalation of the material or due to the coughing up of
inhaled radium followed by ingestion.
Metabolism
Radium is an element and cannot be metabolized (ASTDR, 1990).
The chemical behavior of radium is similar to that of calcium
(Group 2 in the Periodic Table of Elements), and therefore
compounds of radium are deposited in biological systems analogous
to calcium.
Distribution
The ICRP summarized the extensive literature on the distribution
and retention of radium in adult humans (ICRP, 1993). Briefly,
radium absorbed to blood from the GI tract or lungs follows the
behavior of calcium, although the rate of movement between plasma,
bone, and soft tissue, and excretion rates differs between radium
and calcium. Following oral exposure, a large fraction (about 80
percent) of absorbed radium leaves the blood and passes into the
intestines, and is excreted with the feces (ASTDR, 1990). Secretion
into the GI tract is much greater for humans than laboratory
animals. Radium deposits in the bone substantially more than in the
soft tissue. Much of the radium deposited in the bone is returned
to the plasma within a few weeks, but a fraction (initially around
16 percent) is retained and moves out of the bone more slowly,
probably due to bone remodeling (ASTDR, 1990). In mature humans,
skeletal retention of radium may decrease to less than 10 percent
of injected levels after a month. After 25 years, skeletal
retention decreases to about 1 percent. Limited data on humans
suggests that soft tissue radium may represent about 20 percent of
the total radium body burden during the first several weeks after
exposure but represents a much smaller fraction after a longer
time.
A limited amount of information on the biokinetics of radium in
immature humans is available (ICRP, 1993). These data are
supplemented with age-specific data from laboratory animals. The
ICRP used data from beagles combined with the human information to
make estimates of the distribution and retention of radium in
children (ICRP, 1993). These data indicate that radium is retained
to a greater degree in children because the skeleton is growing.
The radium burden in bone acquired during periods of growth tends
to remain higher than the burden acquired by mature bone. Both
deposition and removal of radium appear to be greater in areas of
bone undergoing rapid remodeling. Greater deposition in the young
skeleton causes less systemic radium available for excretion and
soft tissue uptake.
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Excretion
Some data are available to make reasonable estimates of its
elimination from the body. Excretion of radium from the human body
occurs in two phases following oral, inhaled, or injected exposures
(ASTDR, 1990). For all routes, the majority of the excretion is
through feces. Maletskos et al. (1966, 1969) found approximately 80
percent of ingested radium was rapidly eliminated through the
feces. In the second phase, most of the remaining 20 percent was
excreted more slowly in the feces. Fecal to urinary ratios were
reported to be 30-to-1 for intravenous exposure and 10-to-1 for
subcutaneous exposure (Maletskos et al., 1966, 1969).
The radium systemic biokinetic model is described in ICRP
Publication 67 (1993). It is a “calcium-like” bone volume-filling
model. The model incorporates a central blood plasma (RBC)
compartment connected to tissue compartments: skeleton, kidneys,
liver and other soft tissues, and to output compartments: GI tract
and feces, urinary bladder and urine. Figure 1 shows a schematic of
the systemic model. Table 6 summarizes the age-specific transfer
and excretion rates, and f1 values used by the ICRP.
Table 6. Selected Age Specific Transfer Rates (day-1) for the
ICRP’s Radium Biokinetic Model (ICRP, 1993)
AGE 3 mo 1 y 5 y 10 y 15 y Adult Plasma to urinary bladder 0.202
0.444 0.488 0.355 0.210 0.606 Plasma to upper large intestine
7.26 16.0 17.43 12.78 7.55 21.79
Plasma to trabecular bone surface
10.5 6.3 6.22 9.88 14.45 9.72
Plasma to cortical bone surface
42.0 25.2 21.78 29.32 37.35 7.78
Plasma to liver 0.117 0.257 0.280 0.205 0.121 0.350 Plasma to
soft tissue 0 7.56 16.63 18.14 13.31 7.86 22.68 Plasma to soft
tissue 1 2.33 5.13 5.60 4.11 2.43 7.00 Bone surface to plasma 0.578
0.578 0.578 0.578 0.578 0.578 Bone surface to bone volume
exchange
0.116 0.116 0.116 0.116 0.116 0.116
Trabecular and cortical bone volume to plasma
0.00822 0.00822 0.00822 0.00822 0.00822 0.00822
Soft tissue 0 to plasma 2.52 5.54 6.05 4.44 2.62 7.56 Soft
tissue 1 to plasma 0.693 0.693 0.693 0.693 0.693 0.693 F1 0.6 0.3
0.3 0.3 0.3 0.2
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Figure 1. ICRP’s Radium Systemic Biokinetic Model
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Mechanism of Action
Upon internalization of either radionuclide (226Ra and 228Ra),
the decay process for both radionuclides produces enough energy to
ionize and excite molecules in their path. However, radium absorbed
to blood from the GI-tract or lungs follows the behavior of calcium
and is primarily deposited in bone. The radium burden in bone
acquired during periods of growth tends to remain higher than the
burden acquired by mature bone. Both deposition and removal of
radium appear to be greater in areas of bone undergoing rapid
remodeling.
Although the two radionuclides have similar distribution and
absorption characteristics, the energy released during decay is
distinct. Radium-226 has a higher energy and the emission products
travel a larger distance than radium-228. These differences lead to
differences in toxic potency for the two radionuclides.
In general, radiation ionizes cellular atoms and molecules
(i.e., DNA) via direct or indirect actions. Direct ionization of
DNA involves partial or complete energy transfer to one or more
electrons on the molecule while indirect pathways may involve
formation of toxic products such as free radicals, hydrogen
peroxide, hydroperoxy radicals that can diffuse from the site of
formation and interact with their surroundings (ASTDR, 1999). An
ionizing event may have several outcomes: no damage if the ionized
molecule reforms immediately; damage is repaired with no clinical
effects; or the alterations lead to a wide range of biological
responses including carcinogenic and non-carcinogenic endpoints
(ATSDR, 1999).
TOXICOLOGY
Toxicological Effects in Animals and Plants
In general, the acute adverse effects of radium are believed to
be a consequence of the radiation emitted from the radionuclide
itself and its progeny. Because there is already a considerable
amount of information on the acute effects of radiation on humans
derived from studies on the effects of the atomic bomb survivors
and therapeutic uses of radiation, the effects observed following
exposure to radium and its progeny are described in more detail in
the Toxicological Effects in Humans section of this document. The
experimental animal studies conducted with radium do not duplicate
the human effects. The experimental animal studies have instead
concentrated on radium’s most sensitive endpoint, cancer (ATSDR,
1990). Animal studies include acute and chronic exposures in dogs
and rodents. The adverse effects include death, hematological, bone
and kidney damage, immunological and developmental effects, and
cancer.
Acute Toxicity
In 1914, Proescher and Almquest (ASTDR, 1990) observed
fatalities within 7 to 10 days in mice injected with radium
(presumably radium-226) at 2,000 to 4,000 μCi/kg. No other
information was provided. Larkin (1930) reported decreased body
weights,
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hematological changes, marked degenerative changes in bone
marrow and spleen, and damage to liver, kidney, and thymus gland in
rabbits exposed to 15 and 200 mg of radium. Death occurred within
18 days of treatment, averaging 17 days after the start of
exposure.
Similar findings were reported by Whitman (1933), who reported
decreased white blood cells and decreased body weights in Wistar
rats exposed to highly filtered gamma rays from radium. Rats were
exposed to 6 g or less of radium filtered through 1 mm platinum, 1
mm brass, 16 mm lead, and 5 mm celluloid. Exposure times varied
from 0.5 minute to 17 hours (hr) in geometrical progression. The
lethal exposure to radium with filters was between three hr and six
hr.
Other investigators have also reported hematological effects in
mice (Schoeters and Vanderborght, 1981; Schoeters et al., 1983) and
ocular effects in dogs following injections of 226radium (Taylor et
al., 1972). In mice, a depression of hemopoietic cells was reported
following intraperitoneal injections of 17,820 or 22,320 μCi/kg
(660,000 or 827,00 kBq/kg). Taylor et al. (1972) reported loss of
pigment and melanosis and intraocular melanoma formation in dogs
following intravenous administration of radium-226 at doses of
0.062 to1.1 μCi/kg (2.3 to 41 kBq/kg).
Subchronic Toxicity
Because there is already a considerable amount of information on
the subchronic effects of radiation on humans derived from studies
on the effects of the therapeutic uses of radiation and dial
painters, the subchronic effects observed following exposure to
radium and its progeny are described in more detail in the
Subchronic Toxicity section of the Toxicological Effects in Humans
portion of this document.
Genetic Toxicity
No studies were located regarding genotoxic effects of radium in
animals. However, three reports were found in which the
genotoxicity of radium is described. The data are reported in the
Genotoxicity section of the Toxicological Effects in Humans. In
addition, it should be noted that ATSDR considers ionizing
radiation a mutagen (ATSDR, 1997).
Developmental and Reproductive Toxicity
Whitman (1933) reported reproductive and developmental effects
in Wistar rats exposed to highly filtered gamma rays from radium.
Rats were exposed to 6 g or less of radium filtered through 1 mm
platinum, 1 mm brass, 16 mm lead, and 5 mm celluloid. Exposure
times varied from 0.5 minute to 17 hr in geometrical progression.
Radiation exposure of immature females caused delayed opening of
the vagina. In the progeny of the rats exposed 30 minutes or more,
seven abnormalities (absence or reduced size of eye, shortened
tail) occurred in 160 offspring. With rats exposed 20 minutes or
less, one abnormal rat occurred in 91 offspring. In 300 offspring
of normal controls, one abnormal rat occurred.
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Immunotoxicity
No studies were located regarding immunotoxicological effects of
radium in animals.
Neurotoxicity
No studies were located regarding neurotoxic effects of radium
in animals.
Chronic Toxicity and Carcinogenicity
Most studies with experimental animals (primarily Beagle dogs)
following injection of radium have investigated effects on bone,
due to the preferential accumulation and long-term retention of
radium in the skeleton. Scientists demonstrated these effects with
224Ra, 226Ra 26 and 228Ra. Effects on bone shortly after injection
include changes in bone structure (Jee et al., 1969; Momeni et al.,
1976) or hematopoiesis (Schoeters and Vanderborght, 1981). Doses
used in these studies varied from 2.3 kBq/kg to above 24,800
kBq/kg. When animals are followed for a considerably longer portion
of their lifetimes, bone sarcomas were found in all species tested
(ATSDR, 1990; Raabe et al., 1981; Humphreys et al., 1985; Mays et
al., 1987). Studies also report tumors after a single injection of
radium (Taylor, 1983; Kofranek et al., 1985). Leukemias or
lymphomas have been reported following injection, but the
occurrence peaks at low doses (8-16 kBq of 224Ra), lower than the
doses (64 kBq of 224Ra) that cause osteosarcomas (Humphreys et al.,
1985; Muller et al., 1988). The results of the animal studies
confirm the association of bone necrosis and bone sarcomas with
radium exposures in humans, and provide support for an
approximately linear relationship between dose and the incidence of
bone cancer (Wrenn et al., 1985; Mays et al., 1987).
Toxicological Effects in Humans
The principal data concerning human effects of exposure to
radium come from epidemiological studies of workers, mainly women,
employed as radium dial painters. The luminizing industry used
radium-containing paint to make watch dials with numerals that
would glow in the dark. Prior to the mid-1920s, little attention
was paid to limiting radium exposure of workers. A common practice
was sharpening the tip of the paint-laden brush by twisting it in
the corner of the mouth, which led to considerable ingestion of
paint among many workers. Occupational exposure in the dial
industry continued after 1930 but at substantially lower
levels.
Acute Toxicity
No studies were located regarding the acute toxicological
effects of radium in humans. Many of the effects described in the
literature as the result to radium exposure occur due to long-term
exposures. In some cases, although the exposure may have been
acute, the reported effects observed were considered long-term due
to the long half-life of the radionuclides and poor elimination of
the biologically active radionuclide (ATSDR, 1997). Radium-226 and
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Subchronic Toxicity
Keane et al. (1983) investigated bone changes in young radium
dial workers (median age of 18 years) compared to matching controls
with no radium exposure. The subjects in this study ingested radium
over a very short time period (about a year). Because of the
dosimetry of radium (preferential concentration in the bone and
long-term radioactive decay), the effects of the ingested amount
are thought to be relatively independent of the time-course of
exposure (U.S. EPA, 1991). They expressed radium exposure as intake
to blood in μCi of 226Ra and 228Ra. Bone changes expressed as foci
of necrosis were evaluated by examination of x-ray radiographs of
exposed and control women. Keane et al. (1983) found that below 10
μCi intake of either isotope for a period of 1.39 or 1.12 years
(mean duration of radium intake for 226Ra and 228Ra, respectively),
the severity and frequency of bone changes was not statistically
different between the exposed and control groups. They also found
that below 100 μCi total intake, all changes were mild. However,
radiographs are not sensitive to histological changes in bone, and
Keane et al. (1983) did not investigate possible effects on bone
growth, healing, or homeostasis. The U.S. EPA considers the
detected lesions to be an adverse effect (U.S. EPA, 1991).
The U.S. EPA used the Keane et al. (1983) study to calculate a
non-cancer No Observed Adverse Effect Level (NOAEL). Keane et al.
(1983) found that bone changes were not significantly different
from the controls below a total intake to the blood of 10 μCi of
either 226Ra or 228Ra. In agreement with the U.S. EPA, OEHHA used
10 μCi as the initial NOAEL to calculate the final NOAEL. In order
to derive a NOAEL in units of μCi/kg–day, OEHHA assumed that bone
necrosis was a function of radium intake adjusted for body weight
and duration of radium intake. For 226Ra, the derived NOAEL would
be 3.37 x 10-4 μCi/kg-day [10 μCi/(60 kg x 496 days)]. In the case
of 228Ra, the derived NOAEL would be 4.08 x 10-4 μCi/kg-day [10
μCi/(60 kg x 409 days)]. These derived NOAELs were used to
calculate the health-protective concentration.
Mays et al. (1985) briefly discussed non-malignant disease
observed at increased incidence in patients injected with 224Ra.
These diseases included benign bone growths, severe growth
retardation in children, tooth breakage, kidney and liver disease,
and cataracts. No dose-response information was given for these
effects, but the average injected dose was approximately 300
μCi.
Genetic Toxicity
Three studies show that radium causes mutagenic effects in
humans. Muller et al. (1966) examined bone marrow cells from 5
controls and 16 individuals exposed to 226Ra and/or Sr-90. Exposed
individuals had significantly greater incidence of aneuploid cells
and cells with chromosomal aberrations. Boyd et al. (1966) found a
significantly greater incidence of chromosomal aberrations in the
chromosomes of peripheral lymphocytes of 62 radium dial painters
containing radium ranging from non-measurable to 0.56 microcurie of
226Ra, compared to 57 control individuals. This incidence was also
dose related. Hoegerman et al. (1973) found a weak positive
correlation between radium body burden and the frequency of
chromosomal aberrations in 19 dial painters with similar body
burdens.
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Developmental and Reproductive Toxicity
Two studies on radium dial painters suggest possible
reproductive and developmental effects. Polednak (1980)
investigated the fertility of female radium dial painters with
measured radium body burdens. He found that the live birth rate was
significantly lower for women with ovarian doses above 20 rem
compared to doses below 20 rem. This decrease was complicated by
the fact that confounding factors like contraceptive practices were
not accounted for or controlled. Sharpe (1974) reported the case
histories of 42 workers in the radium dial industry. His comparison
showed a decreased number of children born to women exposed to
radium. He also reported birth defects for a child born to one
woman exposed to radium. The number of cases, however, was too
small to attribute these effects to radium exposure.
Immunotoxicity
No studies were located regarding immunotoxicity effects of
radium in humans.
Neurotoxicity
No studies were located regarding neurotoxicity effects of
radium in humans.
Chronic Toxicity
Fatal cases of jaw necrosis and aplastic anemia among women
employed as dial painters were an early indication of the hazards
associated with 226Ra and 228Ra ingestion (Martland, 1931). From
1922 to 1928, 12 deaths occurred due to these causes among dial
painters and chemists employed in the dial painting industry in New
Jersey. Keane et al. (1983) adequately characterized a
dose-response relationship in humans for bone necrosis. In
addition, other non-cancer effects in humans have been reported
with higher doses of radium exposure (Rundo et al., 1986). Rundo et
al. (1986) estimated that the lowest total intake level of radium
associated with a malignancy was 60 μCi or 1.03 μCi/kg based on
women of 58 kg body weight.
Carcinogenicity
Scientists have long recognized that two types of cancer with
very low spontaneous rates, bone sarcomas and head sarcomas, were
elevated in exposed dial workers (U.S. EPA, 1991). Our discussion
focuses on studies that made quantitative evaluations of the
incidence of tumors as a function of ingested dose.
Rundo et al. (1986) reported the rate of bone and head sarcomas
to be significantly higher for radium dial painters. They
identified a total of 64 bone sarcomas and 24 head sarcomas in a
cohort of 4,032 radium dial painters compared to matched
controls.
Rowland et al. (1978) evaluated a cohort of almost 800 female
dial workers. They found 38 bone sarcomas and 17 head sarcomas with
incidence rates ranging from about 1 to 37 sarcomas per 1,000
person years at risk. The highest incidence was above 1,000 μCi
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226Ra + 2.5 μCi 228Ra. No sarcomas were found in the groups
exposed to less than 100 μCi 226Ra. Spontaneous incidence rates for
these two types of sarcomas are less than one case for a cohort of
this size.
In a later study of a subgroup of dial painters, Rowland et al.
(1983) reported bone sarcoma rates as high as 46 sarcomas per 1,000
person years at risk. They observed the higher rates between 500
and 2500 μCi of 226Ra intake.
Rowland et al. (1978) concluded that a microcurie of 228Ra was
about two times as effective at producing bone sarcomas as a
microcurie of 226Ra. In addition, they demonstrated that the
incidence of head carcinomas was associated only with 226Ra
exposure, not with exposure to 228Ra. The National Academy of
Sciences (NAS) explained this association by the accumulation of
radon gas in the mastoid air cells and paranasal sinuses (NAS,
1988). Both 226Ra and 228Ra have radon decay products, but the
half-life of 220Rn, the progeny of 228Ra, is only about 50 seconds,
too short for substantial diffusion to air cells in the skull to
take place.
No conclusive evidence has been found for statistically
significant increases in cancer other than bone sarcomas and head
carcinomas in dial painters (U.S. EPA, 1991). Marginal increases in
breast cancer, multiple myeloma, and leukemia have been noted. The
lack of increased leukemia incidence is unexpected, because the
accumulation of radium in the bone would be expected to provide
substantial irradiation to potentially leukemogenic cells (Mays et
al., 1985). Possible explanations for the lack of increased
leukemia incidence may be non-uniformity of irradiation, lethality
in target cells, low frequency of target cells in irradiated
regions, or an overestimation of leukemia risk coefficients (U.S.
EPA, 1991).
Petersen et al. (1966) studied mortality statistics of almost
one million people in rural communities of Iowa and Illinois who
had an average of 4.7 pCi/L of 226Ra in their drinking water.
Compared to controls, fatalities from bone malignancies were
marginally elevated.
Bean et al. (1982) studied residents of small communities in
Iowa and found increased incidence for four cancers. This increase
was correlated with increasing radium content in the water
supplies. These cancers included bladder and lung cancer in males,
and breast and lung cancer in females. These findings are weakened
by the facts that correlations with indoor radon levels could not
be ruled out, and these cancers were not observed in dial painters
(NAS, 1988).
Lyman et al. (1985) investigated the correlation between radium
content of groundwater and leukemia incidence in Florida. They
found a small but consistent excess of leukemia in high-exposure
areas, but no evidence of a dose-response. The rank correlation
coefficients of 0.56 and 0.45 were observed between the radium
contamination level and the incidence of total leukemia and acute
myeloid leukemia, respectively. Again, the significance of these
results is questioned because increased incidence of leukemia has
not been observed in dial painters (U.S. EPA, 1991).
Related to the issue of radium carcinogenicity are the
carcinogenicity effects due to exposure to low-level ionizing
radiation, in general. Several investigators have recently reported
associations between low-level exposure to ionizing radiation and
mortality
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among nuclear research and production facility workers. Wing et
al. (2000) and Richardson and Wing (1999a,b) studied ninety-eight
multiple myeloma deaths and 391 age-matched controls selected from
the combined roster of 115,143 workers hired before 1979 at
Hanford, Los Alamos National Laboratory, Oak Ridge National
Laboratory, and the Savannah River site. These investigators did
not find an association between lifetime cumulative whole body
ionizing radiation dose and multiple myeloma. However, they did
report a significant effect of age at exposure: dose-response
associations increased in magnitude with exposure age (from 40 to
50).
In addition, Mancuso et al. (1977) and Kneale et al. (1981,
1984) examined the health risks from low-level radiation in workers
engaged in plutonium manufacture at Hanford Works, Washington
State. The authors reported that a lag time was observed, with a
cancer latency of about 25 years, and that the age at exposure was
associated with increased risk with increasing age. Thus, these
data suggest that older individuals may be more sensitive to
ionizing radiation than younger adults.
The current radium data shows that the ingestion of 226Ra and
228Ra has caused bone and head cancers (Mays et al., 1985; NAS,
1988). Radium follows the behavior of calcium and is primarily
deposited in bone. Although there is a suggested greater
sensitivity in older individuals to low-level ionizing radiation,
the radium burden in bone acquired during periods of growth tends
to remain higher than the burden acquired by mature bone. This
would make children the more sensitive population. The nuclear
industry worker exposure studies would not reveal such an effect
because children were not among this population. Thus, no special
consideration was made regarding the potential greater sensitivity
to older individuals.
DOSE-RESPONSE ASSESSMENT
Noncarcinogenic Effects
OEHHA found that the only health effect of radium ingestion with
an adequately characterized dose-response relationship in humans
was bone necrosis, in a study by Keane et al. (1983). Other
non-cancer effects in humans have been reported at higher doses
(Rundo et al., 1986). The U.S. EPA also considers agents emitting
ionizing radiation to be mutagens and teratogens. Several other
studies have confirmed that radium causes bone necrosis using
animal studies (Taylor et al., 1976; Jee et al., 1969; and Momeni
et al., 1976). The NOAELs of μCi total dose from the Keane et al.
(1983) study were used to calculate an average daily dose, based on
the assumption that bone necrosis was a function of radium intake
adjusted for body weight and duration of radium intake (see the
Subchronic Toxicity section). With these assumptions, the derived
NOAELS used in our calculations of the health-protective
concentration were 3.37 x 10-4 μCi/kg-day (337 pCi/kg-day) for
226Ra and 4.08 x 10-4 μCi/kg-day (408 pCi/kg-day) for 228Ra. These
values are used in calculations below to derive health-protective
concentrations in drinking water for non-cancer effects.
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Carcinogenic Effects
The U.S. EPA classifies all emitters of ionizing radiation as
Group A carcinogens based on sufficient epidemiological evidence
(U.S. EPA, 1999). [The reader is encouraged to read this document
and its references in order to better understand U.S. EPA’s
interpretation of carcinogenicity data and mechanisms.] There is
strong human evidence that the ingestion of 226Ra and 228Ra caused
bone and head cancers in radium dial painters (Mays et al., 1985;
NAS, 1988). Patients injected with known amounts of 224Ra had
increased risk of developing bone sarcomas (NAS, 1988). The
dose-response from both the dial painters and the injected patients
was linear (NAS, 1988). In 1999 the U.S. EPA estimated the
radiogenic cancer risks from ionizing radiation and calculated the
overall mortality and morbidity risk to be about 5.75 x 10-4 and
8.46 x 10-4 per rad, respectively (U.S. EPA, 1999).
In the same publication, the U.S. EPA developed carcinogenic
potencies or risk coefficients for almost all radionuclides
including 226Ra and 228Ra. These risk coefficients are listed in
U.S. EPA’s Federal Guidance Report No. 13 (U.S. EPA, 1999). These
risk coefficients apply to an average member of the public in that
estimates of risk are averaged over age and gender distributions of
a hypothetical closed population with an unchanging gender ratio
whose survival functions and cancer mortality rates are based on
the 1989-91 U.S. life table statistics (NCHS, 1997) and U.S. cancer
mortality data for the same period (NCHS, 1992; 1993a,b). The U.S.
EPA provides mortality and morbidity risk coefficients for each
radionuclide and exposure route (inhalation and ingestion of food,
water and soil). For each of the internal exposure modes, the risk
coefficient for a radionuclide includes the contribution to dose
from the production of decay chain members in the body after intake
of the parent radionuclide. The five steps in computing the risk
coefficients for internal exposure are as follows:
• Step 1. Lifetime risk per unit absorbed dose at each age:
Radiation risk models are used to calculate gender-specific
lifetime risks per unit of absorbed dose for 14 cancer sites.
• Step 2. Absorbed dose rates as a function of time post-acute
intake at each age: Age-specific biokinetic models are used to
calculate the time dependent inventories of activity in various
regions of the body following an acute intake of a unit of
radionuclide activity. Six ages are used: 100 days and 1, 5, 10,
15, 20-25 years.
• Step 3. Lifetime cancer risk per unit intake at each age: For
each cancer site, the gender-specific values of lifetime risk per
unit absorbed dose at each age (from the first step) are used to
convert the calculated absorbed dose rates to lifetime cancer risks
for acute intake of one unit of activity at each age xi.
• .Step 4. Lifetime cancer risk for chronic intake: The U.S. EPA
assumed that the concentration of the radionuclide in the
environmental medium remains constant and that all persons in the
population are exposed throughout their lifetimes.
• Step 5. Average lifetime cancer risk per unit activity intake:
Because a risk coefficient is an expression of the radiogenic
cancer risk per unit activity intake, the calculated lifetime
cancer risk from chronic intake of the environmental medium must be
divided by the expected lifetime intake.
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A more detailed explanation of these five steps is presented in
the U.S. EPA’s Federal Guidance Report No. 13 (U.S. EPA, 1999).
Analyses involving the risk coefficients should be limited to
estimation of prospective risks in large existing populations,
rather than being applied to specific individuals. Also the risk
coefficients may not be suitable for assessing the risk to an
average individual in an age-specific cohort. The U.S. EPA
performed all computations of dose and risk using DCAL, a
comprehensive biokinetic-dose-risk computational system designed
for radiation dosimetry (U.S. EPA, 1999). DCAL has been extensively
tested and has been compared with several widely used solvers for
biokinetic models and systems of differential equations. DCAL was
used by a task group of the ICRP to derive or check the dose
coefficients given in it series of documents on age specific doses
to members of the public from the intakes of radionuclides (ICRP,
1989, 1993, 1995, 1996a,b).
The risk coefficients from the Federal Guidance Report No. 13
for 226Ra and 228Ra are listed in Table 7 below for the water
ingestion exposure route (U.S. EPA, 1999) in both units of Bq-1 and
pCi-1.
Table 7. Drinking Water Risk Coefficients for 226Ra and
228Ra
Risk Coefficient a (Bq-1) Risk Coefficient b (pCi-1)
Radionuclide Mortality Morbidity Mortality Morbidity 226Ra 7.17 x
10-9 1.04 x 10-8 2.65 x 10-10 3.85 x 10-10228Ra 2.00 x 10-8 2.81 x
10-8 7.40 x 10-10 1.04 x 10-9
a Values taken from U.S. EPA, 1999 b Converted from Bq-1 to
pCi-1 by multiplying by 0.037 Bq/pCi
The scientific community has been aware for many years of the
possibility that low doses of ionizing radiation may result in
changes in cells and organisms, which reflects an ability to adapt
to the effects of radiation. There is also a suggestion that low
doses of ionizing radiation protect against cancer rather than
conferring cancer risk (radiation hormesis), based both on
experimental results showing adaptive responses and on
interpretations of epidemiological studies, as reported by the
United Nations Scientific Committee on the Effects of Atomic
Radiation (UNSCEAR) (UNSCEAR, 1994; NCRP, 2001).
The National Council on Radiation Protection and Measurements
(NCRP, 2001) reviewed the most recent epidemiological evidence and
concluded that there is no strong support for a hormesis
interpretation of the radiation epidemiological literature. They
conclude that all epidemiological evidence implicating hormesis was
either a statistical anomaly that disappeared as more and better
data became available, or was due to confounding factors such as
better health for radiation workers. The NCRP also concluded that
low-dose cancer studies are equivocal because of the intrinsic
limitations in their precision and statistical power. Because of
these limitations there is a danger in over-interpreting either
individual negative studies or individual highly positive
studies.
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CALCULATION OF PHG Calculations of concentrations of chemical
contaminants in drinking water associated with negligible risks for
carcinogens or non-carcinogens must take into account the toxicity
of the chemical itself, as well as the potential exposure of
individuals using the water. Tap water is used directly as drinking
water, for preparing foods and beverages. It is also used for
bathing or showering, and in washing, flushing toilets and other
household uses, resulting in potential dermal and inhalation
exposures.
Noncarcinogenic Effects
Non-carcinogenic effects due to radium have been characterized
since 1922. Fatal cases of jaw necrosis and aplastic anemia among
women employed as dial painters were reported by Martland (1931).
Keane et al. (1983) characterized the dose-response relationship in
humans for bone necrosis following radium exposure. Furthermore,
bone necrosis has also been reported to occur in animals following
exposure to radium (Taylor et al., 1976; Jee et al., 1969; and
Momeni et al., 1976). The NOAELs based on the Keane et al. (1983)
study were used to calculate the proposed health-protective
concentrations below for radium–226 and radium–228. An uncertainty
factor of 3 was applied in the calculation to correct for less than
lifetime exposure since the data were obtained from individuals
exposed for less than 2 years. In addition, an uncertainty factor
of 3 was used to account for interindividual variability in the
diverse California population. A larger uncertainty factor was not
used for interindividual variability since the data were obtained
from a population whose median age was 18 years; already a
sensitive population for bone necrosis. We calculated the
public-health protective concentration (C) for non-carcinogenic
endpoints using the equation:
C = NOAEL x BW x RSC UF x WC
where:
NOAEL = derived No Observable Adverse Effect Levels are 337
pCi/kg-day 226Ra and 408 pCi/kg-day for 228Ra;
BW = adult body weight of 70 kg, or 10 kg for a child; RSC =
relative source contribution of 0.5, based on the estimated
contribution from foods compared to drinking water; UF =
combined uncertainty factor (3 to account for individual
differences in sensitivity to radium toxicity and 3 for
non-lifetime exposure, multiplied to equal 10 based on the
convention that the two values of 3 each represent half of 10 on a
logarithmic scale);
WC = drinking water ingestion rate for an adult of 2 L/day and a
child of 1 L/day; no component is added for volatilization because
the chemicals are non-volatile, and inhalation of aerosol droplets
in
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showering is considered to provide a negligible added exposure
in this case.
For a child, the calculated health-protective concentration for
the two radionuclides would be as follows:
C = 337 pCi/kg-day x 10 kg x 0.5 = 170 pCi/L for 226Ra 10 x 1
L/day
C = 408 pCi/kg-day x 10 kg x 0.5 = 200 pCi/L for 228Ra 10 x 1
L/day
For an adult, the calculated health-protective concentration for
the two radionuclides would be as follows:
C = 337 pCi/kg-day x 70 kg x 0.5 = 590 pCi/L for 226Ra 10 x 2
L/day
C = 408 pCi/kg-day x 70 kg x 0.5 = 710 pCi/L for 228Ra 10 x 2
L/day
Table 8 lists the calculated health-protective concentrations
(C) for the two radionuclides and ages, based on non-cancer
effects. Additionally, the public health protective concentrations
are expressed in pg/L for comparative purposes. This value is
obtained by dividing the calculated health-protective concentration
in μCi/L by the specific activity for each radionuclide (i.e.,
0.988 pCi/pg and 275 pCi/pg for 226Ra and 228Ra, respectively).
Table 8. Health-Protective Concentrations for Non-cancer Effects
of 226Ra and 228Ra
Health Protective Concentrations Child Adult
Radionuclide
pCi/L pg/L pCi/L pg/L 226Ra 170 170 590 600 228Ra 200 0.75 710
2.6
We conclude that appropriate concentrations to protect against
non-cancer effects of these isotopes are 200 pCi/L of either
isotope, corresponding to 200 pg/L of 226Ra and 1 pg/L of 228Ra
(all values rounded to one significant figure). These public health
Radium-226 and 228 in Drinking Water California Public Health Goal
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protective concentrations are much higher than the one derived
below for cancer. Therefore the drinking water concentration
estimated below to protect against carcinogenic effects is also
protective against non-cancer chronic toxicity.
Carcinogenic Effects
There is strong human evidence that ingestion of 226Ra and 228Ra
caused bone and head cancers in radium dial painters (Mays et al.,
1985; NAS, 1988). Patients injected with known amounts of 224Ra had
increased risk of developing bone sarcomas (NAS, 1988). The
dose-response from both dial painters and injected patients was
linear (NAS, 1988). The U.S. EPA developed carcinogenic potencies
or risk coefficients for almost all radionuclides, including 226Ra
and 228Ra. The risk coefficients for 226Ra and 228Ra are listed in
Table 7 and are based on the findings of the U.S. EPA’s Federal
Guidance Report No. 13 (U.S. EPA, 1999). For calculating the
health-protective concentration for 226Ra and 228Ra, the morbidity
risk coefficients were used in our calculations. The morbidity risk
coefficient is an estimate of the average total risk of
experiencing a radiogenic cancer, whether or not the cancer is
fatal. We calculated the drinking water concentration corresponding
to a de minimis cancer morbidity risk (1 in 1 million) using the
following equation for each radionuclide.
C = R EP x CRC x WC
where:
R = de minimis cancer risk of one in a million; EP = exposure
period of 70 years (25,568 days); CRC = morbidity cancer risk
coefficients (pCi-1) 226Ra = 3.85 x 10-10,
228Ra = 1.04 x 10-9; WC = drinking water ingestion rate (2
L/day).
The health-protective concentration of 226Ra is therefore
calculated as:
C = 10-6 = 0.05 pCi/L 25,568 d x 3.85 x 10-10 pCi-1 x 2 L/d
The health-protective concentration of 228Ra is calculated
as:
C = 10-6 = 0.019 pCi/L 25,568 d x 1.04 x 10-9 pCi-1 x 2 L/d
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Because the cancer values are much lower and more
health-protective than the non-cancer values, the PHG is set at the
health-protective values for the cancer endpoint. These values,
0.05 pCi/L for 226Ra and 0.019 pCi/L for 228Ra, correspond to a 1
in one million upper-bound lifetime cancer morbidity risk for each
of the isotopes. At these radioactivity levels in water,
individuals, including sensitive subpopulations, should also be
protected against the non-cancer effects of the isotopes.
RISK CHARACTERIZATION The primary sources of uncertainty in the
development of the PHG for radium-226 and radium-228 in drinking
water include some of the general issues of uncertainty in any risk
assessment, particularly dose-response modeling and estimation of
exposures. However, there is a considerable amount of certainty in
key areas of the risk assessment of radium, including the mode of
action, inter- and intra-species extrapolation, and relative source
contribution (RSC). A substantial body of information exists on the
carcinogenic effects of radionuclides, including radium, on human
subjects. U.S. EPA as well as other entities have developed and are
perfecting models to estimate human body exposures to
radionuclides, which have also added to the certainty of the
estimations.
The PHGs for radium-226 and radium-228 are 0.05 and 0.019 pCi/L,
respectively. These estimated protective health concentrations were
calculated based on the carcinogenic potencies of 3.85 x 10-10 and
1.04 x 10-9 per pCi, respectively, developed by U.S. EPA (1998). In
calculating the PHG values, a de minimis excess individual cancer
risk level of 10-6 was used, which is applied to all chemicals for
which a non-threshold cancer risk assessment is judged to be
relevant, to meet the intent of the statute. The corresponding
levels for lifetime cancer risks of 10-5 or 10-4 are 0.5 pCi/L and
5.0 pCi/L, respectively, for radium 226. For radium-228, the
corresponding levels for lifetime cancer risks of 10-5 or 10-4 are
0.19 pCi/L and 1.9 pCi/L, respectively.
No additional assumptions are needed with respect to the use of
RSCs for radium. The U.S. EPA’s risk value is specific for
ingestion of radium in water.
OTHER REGULATORY STANDARDS As early as 1928, both the
international and U.S. radiation protection community established
agencies to ensure the safe use of ionizing radiation. These
agencies are now called the International Commission on
Radiological Protection (ICRP) and the National Council on
Radiation Protection and Measurements (NCRP).
The NCRP was chartered by the U.S. Congress to (1) disseminate
information of public interest and recommend radiation levels to
protect the public, (2) support cooperation among organizations
concerned with radiation protection, (3) develop basic concepts
about radiation protection, and (4) cooperate with the ICRP. Even
though the NCRP is a nongovernmental organization, it guides the
establishment of federal radiation policies, requirements, and
statutes. Based on the recommendation of the NCRP, the U.S. EPA
sets radiation protection policy and guidance for all of the
federal governmental agencies and state cooperating radiation
safety programs.
Radium-226 and 228 in Drinking Water California Public Health
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The federal government has several different agencies that
regulate the safe use of radioactive material. The Nuclear
Regulatory Commission (NRC) regulates commercial power reactors,
research and test reactors, nuclear fuel cycle facilities, and the
transport, storage, and disposal of nuclear materials and waste.
The U.S. EPA regulates the individual radiation dose for the
nuclear fuel cycle, the level of radionuclides emitted to the air
and in drinking water, along with residual levels of radiation at
uranium and thorium mills, and the release of radionuclides from
high-level waste disposal facilities. The Food and Drug
Administration (FDA) develops standards for equipment that emits
ionizing radiation, and the Department of Transportation (DOT), in
conjunction with the NRC, regulates the transport of radioactive
material. All these agencies follow the recommendations of the
NCRP.
Table 9 summarizes the international and national guidelines and
standards pertinent to human exposure to ionizing radiation and
Radium-226. These include the guidelines from the ICRP and NCRP,
relevant federal standards from the NRC, U.S. EPA, and the DOT. We
also include current state standards applicable to Radium-226 in
drinking water (Table 10).
Table 9. Relevant Radiation Protection Guidelines and
Regulations (from ATSDR 2001)
Agency Description Guideline or Regulation ICRP Guideline dose
for the protection of the
general public 100 mrem/year
NCRP Guideline dose for the protection of the general public
100 mrem/year
NCRP Guideline dose for any individual radiation source or
practice
10 mrem/year
NRC Regulation for the protection of the general public
100 mrem/year (10 CFR 20.1301)
NRC Regulation for the protection of the general public –
Low-level Radioactive Waste Disposal Facilities
25 mrem/year (10 CFR 61)
NRC Regulation for the protection of the general public-
Decommissioned Facilities
25 mrem/year (10 CFR 20)
U.S. EPA Regulation. Maximum Contaminant Level in community
water systems Radium-226, Radium-228, and alpha particle: Beta
particle and photon activity:
5 pCi/L (40 CFR 141.15) 4 rem/year (40 CFR 141.16)
DOT Regulation for transport in normally occupied space.
2 mrem/hour (49 CFR 173)
*- CFR – Code of Federal Regulations
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The federal government has regulated the levels of 226Ra and
228Ra in community water supplies since the mid-1970s. The U.S. EPA
promulgated Maximum Contaminant Levels (MCLs) for radium and other
radionuclides in community water supplies in their 1976 National
Interim Primary Drinking Water Regulation (U.S. EPA, 1976). The
combined MCL for 226Ra and 228Ra is 5 pCi/L.
In 1991, the U.S. EPA proposed new MCLs for 226Ra and 228Ra at
20 pCi/L each based on newer dosimetry (U.S. EPA, 1991). They based
the MCLs on a 4 mrem/year effective dose equivalent using the
RADRISK Computer Code and 2 L/day drinking water rate. The proposed
rule was never implemented.
In 2000, the U.S. EPA finalized their rule for drinking water
(U.S. EPA, 2000, 2002). For 226Ra and 228Ra the MCL remains at 5
pCi/L (combined) because updated dosimetry and risk levels yielded
similar concentrations (U.S. EPA, 2005a). This MCL is scheduled for
review in the next 2 to 3 years for risk management issues.
California adopted the U.S. EPA MCL of 5 pCi/L for the combined
radionuclides in 1997, and this MCL is still in force (DHS,
2005d).
Table 10. State Regulations for Radium-226 in Drinking Water
(ATSDR, 2001)
State or Territory Standard (pCi/L) Alabama, Alaska, California,
Colorado, Connecticut, Florida, Iowa, Indiana, Rhode Island,
Utah
5
New York, Puerto Rico, Washington, Wyoming 3
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